Abstract
The stomach is the primary source of the orexigenic and adiposity-promoting hormone, ghrelin. There is emerging evidence on the nutrient-mediated modulation of gastric ghrelin secretion. However, limited information is available on gastric nutrient-sensing mechanisms in high-fat diet (HFD)-induced obesity. This study investigated the impact of HFD-induced obesity on the expression of nutrient chemosensors in mouse stomach, particularly ghrelin cells. Male C57BL/6 mice were fed either a standard laboratory diet (SLD) or HFD for 12 weeks. The expression of ghrelin, enzymes involved in ghrelin production (PC1/3, GOAT) and nutrient chemosensors (CD36, FFAR2&4, GPR93, CaSR, mGluR4 and T1R3) was determined by quantitative RT-PCR in the mouse corpus and antrum. Immunohistochemistry assessed the protein expression of CaSR and ghrelin in the corpus and antrum. Antral mRNA levels of CaSR and PC1/3 were increased in HFD compared to SLD mice, while mRNA levels of all other nutrient chemosensors examined remained unchanged. CaSR immunolabelling was observed in the gastric antrum only. Nearly 80% of antral ghrelin cells expressed CaSR, with a similar cell density and co-expression in SLD and HFD mice. In conclusion, HFD-induced obesity increased CaSR mRNA expression in mouse antrum. However, the high antral co-expression of CaSR and ghrelin was unaltered in HFD compared to SLD mice.
Highlights
Obesity is a global health issue characterized by an excessive body weight (i.e., body mass index (BMI) ≥ 30 kg/m2 ) and accompanying metabolic disorders, such as type 2 diabetes and cardiovascular disease [1]
The current study found that high-fat diet (HFD)-induced obesity did not alter the mRNA expression of ghrelin and a wide range of nutrient chemosensors in the mouse stomach
Most nutrient chemosensors investigated in this report had a comparable mRNA expression in lean and HFD-induced obese mice
Summary
Obesity is a global health issue characterized by an excessive body weight (i.e., body mass index (BMI) ≥ 30 kg/m2 ) and accompanying metabolic disorders, such as type 2 diabetes and cardiovascular disease [1]. Obesity is primarily caused by a chronic energy imbalance, often resulting from increased consumption of energy-dense foods that are rich in fat and sugars [1]. A better understanding of the mechanisms controlling food intake is essential for the development of strategies for the treatment of obesity. In this context, research focused on gastrointestinal hormones that modulate appetite and energy metabolism has exponentially increased. Ghrelin is a gastrointestinal hormone with an important role in body energy homeostasis, stimulating food intake and adiposity [2,3]. Ghrelin is primarily produced by P/D1 (human) and
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